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Background: Multiple studies have uncovered the effects that ingested fat has on human blood levels of testosterone. Yet, few reports have discussed the effect of circulating serum free fatty acids (FFAs). The present study aimed to explore the relationship between serum free fatty acids and blood levels of testosterone. Methods: In total, 5719 adults were pooled from the database of the National Health and Nutrition Examination Survey (NHANES) from 2011 to 2012. Based on multivariable‐linear regression models, we employed a total of 30 FFAs to interpret the relationship of FFAs with blood levels of testosterone. Two models with covariate adjustments were designated for further evaluation and analysis. Results: Capric acid [β = −0.014, 95% confidence interval (CI) = −0.023, −0.004, P = 0.005], myristic acid (β = −0.001, 95% CI = −0.001, 0.000, P ≤ 0.001), pentadecanoic acid (β = −0.013, 95% CI = −0.018, −0.008, P ≤ 0.001), margaric acid (β = −0.011, 95% CI = −0.017, −0.005, P ≤ 0.001) and alpha‐linolenic acid (β = −0.001, 95% CI = −0.002, 0.000, P = 0.004) in the fully adjusted model were significantly negatively correlated with the testosterone level inh obese men. In the fully adjusted model for the female analysis, myristic acid, pentadecanoic acid, palmitic acid, margaric acid, stearic acid, myristoleic acid, oleic acid, nervonic acid and alpha‐linolenic acid were found significantly associated with the testosterone level. Conclusions: Our findings indicate a significant negative correlation between serum FFAs and blood levels of testosterone. Furthermore, we reveal the essentiality of serum FFAs and their potential effects on the reduction of testosterone levels. [ABSTRACT FROM AUTHOR]

Summary: The kinetics of serum hepatitis B surface antigen (HBsAg) during the natural history of hepatitis B virus (HBV) infection has been studied, but the factors affecting them remain unclear. We aimed to investigate the factors affecting HBsAg titres, using data from multicentre, large‐sized clinical trials in China. The baseline data of 1795 patients in 3 multicentre trials were studied, and the patients were classified into 3 groups: hepatitis B early antigen (HBeAg)‐positive chronic HBV infection (n = 588), HBeAg‐positive chronic hepatitis B (n = 596), and HBeAg‐negative chronic hepatitis B (n = 611). HBsAg titres in the different phases were compared, and multiple linear progression analyses were performed to investigate the implicated factors. HBsAg titres varied significantly in different phases (P = .000), with the highest (4.60 log10 IU/mL [10%‐90% confidence interval: 3.52 log10 IU/mL‐4.99 log10 IU/mL]) in patients with HBeAg‐positive chronic HBV infection. In all phases, age and HBV DNA were correlated with serum HBsAg level. In HBeAg‐positive chronic hepatitis B patients, a negative correlation between HBsAg titres and fibrosis stage was observed. Alanine amonitransferase or necroinflammatory activity was also correlated with HBsAg titres in HBeAg‐negative chronic hepatitis B patients. In conclusion, decreased HBsAg titres may be associated with advancing fibrosis in HBeAg‐positive chronic hepatitis B patients or increased necroinflammation in those with HBeAg‐negative chronic hepatitis B. Our findings may help clinicians better understand the kinetics of HBsAg and provide useful insights into the management of this disease. [ABSTRACT FROM AUTHOR]

Background Many strategies are used to prevent nonsteroidal anti-inflammatory drug ( NSAID)-associated gastrointestinal toxicity, but the comparative effectiveness remains unclear. Aim To evaluate the comparative effectiveness of clinical strategies for preventing gastrointestinal toxicity induced by NSAIDs. Methods MEDLINE, EMBASE and the Cochrane Library (from their inception to May 2015) were searched for randomised controlled trials comparing the risk of gastrointestinal adverse events in patients taking nonselective NSAIDs, selective cyclooxygenase( COX)-2 inhibitors or nonselective NSAIDs/ COX-2 inhibitors plus gastroprotective agents [proton pump inhibitors ( PPIs), histamine-2 receptor antagonists, misoprostol]. Both pairwise meta-analysis and Bayesian network meta-analysis were performed. Results Analyses were based on 82 trials including 125 053 participants. Network meta-analysis demonstrated that selective COX-2 inhibitors + PPIs [Risk ratio ( RR), 95% Credible Interval (CrI): ulcer complications 0.07, 0.02-0.18], selective COX-2 inhibitors ( RR, 95% CrI: ulcer complications 0.25, 0.15- 0.38; symptomatic ulcer 0.12, 0.04-0.30), nonselective NSAIDs + PPIs ( RR, 95% CrI: ulcer complications 0.28, 0.18-0.41; symptomatic ulcer 0.11, 0.04-0.23), nonselective NSAIDs + misoprostol ( RR, 95% CrI: ulcer complications 0.47, 0.24-0.81; symptomatic ulcer 0.41, 0.13-1.00) were associated with significantly lower risk of clinical gastrointestinal events compared with nonselective NSAIDs. For all effectiveness endpoints, selective COX-2 inhibitors + PPIs was associated with the lowest absolute event probability and the highest rank, followed by selective COX-2 inhibitors and thirdly by nonselective NSAIDs + PPIs. Conclusion The combination of selective COX-2 inhibitors plus PPIs provides the best gastrointestinal protection, followed by selective COX-2 inhibitors, and thirdly by nonselective NSAIDs plus PPIs. [ABSTRACT FROM AUTHOR]

Aim: Given the unclear pattern of cerebral function reorganization induced by spinal cord injury (SCI), this study aimed to longitudinally evaluate the changes in resting-state functional connectivity (FC) in the sensorimotor network after SCI and explore their relationship with gait performance., Methods: Four adult female rhesus monkeys were examined using resting-state functional magnetic resonance imaging during their healthy stage and after hemitransected SCI (4, 8 and 12 weeks after SCI), and the gait characteristics of their hindlimbs were recorded (except 4 weeks after SCI). Twenty sensorimotor-related cortical areas were adopted in the FC analysis to evaluate the functional network reorganization. Correlation analyses were then used to explore the relationship between functional network variations and gait characteristic changes., Results: Compared with that during the healthy stage, the FC strength during post-SCI period was significantly increased in multiple areas of the motor control network, including the primary sensorimotor cortex, supplementary motor area (SMA) and putamen (Pu). However, the FC strength was remarkably reduced in the thalamus and parieto-occipital association cortex of the sensory network 8 weeks after SCI. Most FC intensities gradually approached the normal level 12 weeks after the SCI. Correlation analyses revealed that the enhanced FC strength between Pu and SMA in the left hemisphere, which regulates motor functions of the right side, was negatively correlated with the gait height of the right hindlimb., Conclusion: The cerebral functional network presents an adjust-recover pattern after SCI, which may help us further understand the cerebral function reorganization after SCI., (© 2015 Scandinavian Physiological Society. Published by John Wiley & Sons Ltd.)